Jeong Ji-Soo, Kim Jeong-Won, Kim Jin-Hwa, Kim Chang-Yeop, Ko Je-Won, Kim Tae-Won
College of Veterinary Medicine (BK21 FOUR Program), Chungnam National University, Daejeon, Republic of Korea.
J Ginseng Res. 2024 Jan;48(1):52-58. doi: 10.1016/j.jgr.2023.07.002. Epub 2023 Jul 5.
Skeletal muscle denervation leads to motor neuron degeneration, which in turn reduces muscle fiber volumes. Recent studies have revealed that apoptosis plays a role in regulating denervation-associated pathologic muscle wasting. Korean red ginseng (KRG) has various biological activities and is currently widely consumed as a medicinal product worldwide. Among them, ginseng has protective effects against muscle atrophy in and . However, the effects of KRG on denervation-induced muscle damage have not been fully elucidated.
We induced skeletal muscle atrophy in mice by dissecting the sciatic nerves, administered KRG, and then analyzed the muscles. KRG was administered to the mice once daily for 3 weeks at 100 and 400 mg/kg/day doses after operation.
KRG treatment significantly increased skeletal muscle weight and tibialis anterior (TA) muscle fiber volume in injured areas and reduced histological alterations in TA muscle. In addition, KRG treatment reduced denervation-induced apoptotic changes in TA muscle. KRG attenuated p53/Bax/cytochrome c/Caspase 3 signaling induced by nerve injury in a dose-dependent manner. Also, KRG decreases protein kinase B/mammalian target of rapamycin pathway, reducing restorative myogenesis.
Thus, KRG has potential protective role against denervation-induced muscle atrophy. The effect of KRG treatment was accompanied by reduced levels of mitochondria-associated apoptosis.
骨骼肌去神经支配会导致运动神经元变性,进而减少肌纤维体积。最近的研究表明,细胞凋亡在调节去神经支配相关的病理性肌肉萎缩中起作用。韩国红参(KRG)具有多种生物活性,目前在全球作为一种药品被广泛食用。其中,人参对[具体情况1]和[具体情况2]中的肌肉萎缩具有保护作用。然而,KRG对去神经支配诱导的肌肉损伤的影响尚未完全阐明。
我们通过切断坐骨神经诱导小鼠骨骼肌萎缩,给予KRG,然后对肌肉进行分析。术后以100和400毫克/千克/天的剂量给小鼠每日一次注射KRG,持续3周。
KRG治疗显著增加了损伤区域的骨骼肌重量和胫前(TA)肌纤维体积,并减少了TA肌肉的组织学改变。此外,KRG治疗减少了TA肌肉中去神经支配诱导的细胞凋亡变化。KRG以剂量依赖的方式减弱了神经损伤诱导的p53/Bax/细胞色素c/半胱天冬酶3信号传导。此外,KRG降低了蛋白激酶B/雷帕霉素哺乳动物靶标途径,减少了修复性肌生成。
因此,KRG对去神经支配诱导的肌肉萎缩具有潜在的保护作用。KRG治疗的效果伴随着线粒体相关凋亡水平的降低。